eIF3i促进了NELFCD转化,通过调节EMT和侵入来促进转移
Qing Huang1, Juan Zhao2,3, Yang Zhang1
1Laboratory of Gastrointestinal Tumor Epigenetics and Genomics, State Key Laboratory of Biotherapy and Cancer Center, and Frontiers Science Center for Disease-related Molecular Network, West China Hospital, Sichuan University, Chengdu, PR China.
British journal of cancer
|November 28, 2025
概括
eIF3i-NELFCD通路通过促进NELFCD转化,促进细胞入侵和上皮-介质细胞过渡 (EMT) 来驱动结直肠癌 (CRC) 转移. 针对这一轴提供了一个新的策略来防止CRC传播.
科学领域:
- 分子生物学分子生物学
- 癌症研究 癌症研究
- 翻译性重编程是一种翻译性重编程.
背景情况:
- 翻译重编程是癌症进展和转移的关键.
- 对于eIF3i在促进瘤转移中的作用尚不完全理解.
研究的目的:
- 阐明eIF3i促进结直肠癌 (CRC) 转移的机制.
- 为了确定涉及转移的eIF3i的下游目标.
主要方法:
- 蛋白质组分析以确定eIF3i目标.
- 在体外和体外的功能测定 (迁移,入侵,多体样化,RNA结合测定,小鼠模型).
- 在CRC患者肝转移的临床评估.
主要成果:
- eIF3i过度表达与转移性CRC相关,并促进迁移,入侵,EMT和转移.
- NELFCD被确定为直接下游目标,eIF3i促进其翻译.
- NELFCD的淘汰模仿了eIF3i的消耗效应;同时淘汰取消了eIF3i的转移性作用.
- 在临床CRC转移中,eIF3i和NELFCD蛋白水平之间的正相关性.
结论:
- eIF3i-NELFCD轴通过增强的NELFCD转化驱动CRC转移,促进EMT和invadopodia形成.
- 这一途径是抑制CRC转移的潜在治疗标.
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